Dobutamine inhibits vasopressin-mediated water transport across toad bladder epithelium

This study aimed to investigate the effect of dobutamine on water transport across toad bladder epithelium. Water flow through the membrane was measured gravimetrically in bladder sac preparations. Dobutamine had no effect on basal water transport, but partially inhibited transport stimulated by vasopressin. Similarly, dobutamine exerted no influence on the hydrosmotic response to 8-chlorophenylthio-cAMP, but interfered with the response to phosphodiesterase inhibitor 1-methyl-3-isobutyl-xanthine. These results demonstrate that this catecholamine may inhibit vasopressin-stimulated water transport at a site prior to cAMP formation. The use of propranolol was ineffective in blocking the effect of dobutamine on transport stimulated by vasopressin, indicating that β-adrenoceptors play no role in this effect. On the other hand, phentolamine significantly reduced the effect of dobutamine, indicating the involvement of α-adrenoceptors in such event. Rauwolscine also inhibited the effect of dobutamine, pointing to the specific contribution of the α2-adrenoceptors to this effect. Taken together, the results of this study demonstrate that dobutamine inhibits vasopressin-stimulated water transport in toad bladders through a mechanism mediated by the stimulation of α2-adrenoceptors, thus suggesting that such a drug may exert a direct cellular effect on membrane permeability to water in transporting epithelia. The current study may provide a better understanding of the effects of dobutamine on renal function by contributing towards the elucidation of its action mechanism.